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Instituto Evandro Chagas

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Actividad rítmica espontánea en vasos de placenta humana: ¿un marcapaso fisiológico en los vasos sanguíneos? / Spontaneous rhythmic contractions of human umbilical vessels, evidences for a physiological pacemaker in blood vessels?

Huidobro Toro, Juan Pablo; González C., Rolando; Varas F., José Alejandro; Rahmer Ovalle, Alejandro; González Aldunate, Rolando.
Rev. méd. Chile ; 129(10): 1105-1112, oct. 2001. ilus, tab
Artigo em Espanhol | LILACS | ID: lil-301901

Background:

Placental vessels are not innervated. Therefore the vasomotor activity and vascular tone is not regulated by the nervous system.

Aim:

To assess the existence of pacemaker mechanisms related to rhythmic motor activity of blood vessels. Material and

methods:

Isometric contractions of rings from umbilical and chorionic vessels of term human placentas were monitored.

Results:

Recordings of the circular layer of chorionic and umbilical vessels revealed rhythmic spontaneous contractions with a frequency of 1,4ñ0,05 cycles/min, the duration of each cycle was 42,8ñ0,24 s (n=12). The amplitude of contractions was larger in veins than in arteries, predominating in umbilical vein biopsies, proximal to the fetus. Both the frequency and the amplitude of contractions were relatively constant during the first 30 min. However, after an hour, the frequency declined while the amplitude increased. The absence of the endothelium neither modified the frequency nor the amplitude of the rhythmic activity. Blockage of voltage dependent sodium channels or calcium channels did not alter the frequency of spontaneous contractions, although their magnitude was reduced. Glibenclamide, an ATP-dependent K+ channel blocker or the blockade of gap junctions ablated the frequency and amplitude of spontaneous contractions.

Conclusions:

We propose that rhythmic contractions are triggered by pacemaker cells located in the circular layer of the smooth muscle of blood vessels and spread via gap junctions; they likely contribute to the control of blood flow
Biblioteca responsável: CL1.1